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Adenovirus-mediated E2F-1 gene transfer in nonsmall-cell lung cancer induces cell growth arrest and apoptosis

¹ Dept of Pneumology, Medical Clinic I, University Leipzig, ² Dept of Pneumology, Division of Cardiology, Pneumology and Angiology, ³ Dept of Haematology, Oncology and Tumour Immunology, Robert-Rössle-Klinik, University Medical Centre Charité, Humboldt University of Berlin, Berlin, Germany. ⁴ GenVec Inc., Gaithersburg, MD, USA

CORRESPONDENCE: H. Kuhn, Medical Clinic I, University Leipzig, Johannisallee 32, 04103 – Leipzig. Fax: 49 3419712689. E-mail: kuhnh@medizin.uni-leipzig.de

Keywords: E2F-1, gene therapy, nonsmall-cell lung carcinoma, p53

Received: November 10, 2001
Accepted February 10, 2002

Since overexpression of E2F-1 has been shown to induce apoptosis, the ability of adenovirus-mediated transfer of E2F-1 to inhibit tumour growth in nonsmall-cell lung cancer cell lines was investigated.

Three cell lines with various genomic status were infected with AdE2F. Cell proliferation and viability were determined by trypan blue exclusion. Apoptosis induction was assessed by flow cytometry and poly-adenosine diphosphate-ribose-polymerase cleavage assay. In vivo, the effect of E2F-1 on tumour growth was determined in severe combined immunodeficiency (SCID) mice.

The current experiments showed that overexpression of E2F-1 suppressed tumour cell growth. The population of apoptotic cells was dramatically increased 96 h after infection with AdE2F. Inhibition of cell growth and induction of apoptosis was not dependent on genomic status. Moreover, treatment of implanted tumours in SCID mice with AdE2F inhibited tumour growth.

These data suggest that adenovirus-mediated E2F-1 gene therapy may be effective in the treatment of nonsmall-cell lung cancer.